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. 1976 Jan-Feb;71(1):87-95.
doi: 10.1007/BF01907786.

[Potassium-dependent modification of the lidocaine effect: an experimental investigation (author's transl)]

[Article in German]

[Potassium-dependent modification of the lidocaine effect: an experimental investigation (author's transl)]

[Article in German]
K W Diederich et al. Basic Res Cardiol. 1976 Jan-Feb.

Abstract

Lidocaine was supplied to 10 cats by 2 comparative infusions of 7.5 mg/kg respectively. Once the drug was dissolved in a physiological and the other time in a K-Mg-concentrated electrolyte solution. The sequence of both infusions alternated. Serum potassium remained constant during infusion of the physiological electrolyte solution, but increased by about 1 mEqu/1 under K-concentrated solution. Lidocaine caused an enhancement of ventricular fibrillation threshold to an absolutely identical degree in both groups. Increase in cardiac output and stroke volume and decrease of sinus rate was significant in both groups, but more pronounced under K-Mg concentrated solution. Mean arterial pressure, peripheral vascular resistance, PQ, QRS, and QT interval remained constant on the whole. We deduce from these results for antiarrhythmic therapy on normokalemic patients, that the addition of potassium and magnesium to lidocaine solution does not enhance its antifibrillatory effect. This statement is valid for doses up to 20 mEqu/h of magnesium and 40 mEqu/h of potassium.

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